Abstract

B The prevalence, clinical features and incidence of thrombotic microangiopathy (TMA) after renal transplantation are not yet described in literature. M Between 1991 and 2011, 2358 kidney transplants were performed in adult recipients in a single transplant center. All clinical data were prospectively collected and maintained in a dedicated database. We retrospectively identified all patients with features of TMA and evaluated the clinical presentation, prevalence and outcome. R From the total cohort of 2358 patients, 72 (3.0%) were identified with TMA in the post-transplant period (based on the presence schistocytes in a blood smear, suppressed haptoglobin levels, with or without thrombi in a renal biopsy). The clinical presentation was variable: 65 patients (90%) developed anemia, 54 (75%) had thrombocytopenia. Increased bilirubin levels were seen in 23 (32%) patients and an elevated LDH in 69 (95%) of patients. Of the 72 patients diagnosed with TMA after transplantation, 7 were caused by a recurrence of atypical hemolytic uremic syndrome, 1 case was explained by a flare of sickle cell anemia, 1 case was likely associated with sirolimus toxicity, 2 cases were associated with severe opportunistic infections (1 PCP, 1 invasive Aspergillus infection). In 41 patients, there were reported concomitant bacterial infections. In 65 patients, renal allograft biopsies were available at time of TMA. Acute T cell mediated rejection was diagnosed in 44 patients (67.7%), acute antibody-mediated rejection in 7 (11%) of patients with TMA. 51 (70.8%) patients were treated with a calcineurin inhibitor. In 18 patients (25%), TMA was associated with a single potential etiology; in 30 patients (42%) multiple underlying conditions could have explained the occurrence of TMA. In 24 cases (33.3%) there was no clear cause detectable apart from the use of a CNI in 20 cases (27.7%). Of the 72 patients with TMA, 8 (11.1%) patients underwent plasmapheresis and 29 (40%) needed dialysis treatment. Graft loss occurred in 44 (61.1%) patients, with a mean post-tx graft survival of 3.2 ± 1.2 years. C Thrombotic microangiopathy after kidney transplantation is a rare but clinically relevant condition with a very diverse clinical presentation. The etiology is often multifactorial, but in a substantial number of cases no clear cause can be identified. The majority of patients with TMA loose graft function within the first few years after transplantation.

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